Our current understanding of the unstable coronary syndromes is that they fall on a spectrum of disease and begin with a coronary plaque rupture. The degree of thrombus determines the severity of the clinical syndrome, with total occlusion in ST elevation myocardial infarction (MI) or severe (90%) stenosis in patients with non-ST elevation MI or unstable angina. In addition, it is worthwhile to note that 99% of all plaque ruptures are clinically silent. A small degree of rupture leads to a small thrombus, which heals over, but leads to progression of the plaque—like rings on a tree. This is the understanding of how atherosclerosis progresses. This emphasizes the key role that antithrombotic therapy plays in all, patients with unstable coronary syndromes, both acutely and chronically.

ST elevation ST segment elevation usually occurs in the early stages of infarction, and may exhibit quite a dramatic change. ST elevation is often upward and concave, although it can appear convex or horizontal. These changes occur in leads facing the infarction. ST elevation is not unique to MIs and therefore is not confirming evidence. Basic requirements of ST changes for diagnosis are: elevation of at least 1 mm in two or more adjoining leads for inferior infarctions (II, III, and aVF), and at least 2 mm in two or more precordial leads for anterior infarction. You should be aware that ST elevation can be seen in leads V1 and V2 normally. However, if there is also elevation in V3 the cause is unlikely to be physiological.

Deep Q wave The only diagnostic changes of acute myocardial infarction are changes in the QRS complexes and the development of abnormal Q waves. However, this may be a late change and so is not useful for the diagnosis of AMI in the pre-hospital situation. Remember that Q waves of more than 0.04 seconds , or 1 little square, are not generally seen in leads I, II or the precordial leads.

T wave inversion The T wave is the most unstable feature of the ECG tracing and changes occur very frequently under normal circumstances, limiting their diagnostic value. Subtle changes in T waves are often the earliest signs of myocardial infarction. However, their value is limited for the reason above, but for approximately 20 to 30% of patients presenting with MI, a T wave abnormality is the only ECG sign. The T wave can be lengthened or heightened by coronary insufficiency. T wave inversion is a late change in the ECG and tends to appear as the ST elevation is returning to normal. As the ST segment returns towards the isoelectric line, the T wave also decreases in amplitude and eventually inverts.

Bundle branch block Bundle branch block is the pattern produced when either the right bundle or the entire left bundle fails to conduct an impulse normally. The ventricle on the side of the failed bundle branch must be depolarised by the spread of a wave of depolarisation through ventricular muscle from the unaffected side. This is obviously a much slower process and usually the QRS duration is prolonged to at least 0.12 seconds (for right bundle branch block) and 0.14 seconds (for left bundle branch block). The ECG pattern of left bundle branch block (LBBB) resembles that of anterior infarction, but the distinction can readily be made in nearly all cases. Most importantly, in LBBB the QRS is widened to 140 ms or more. With rare exceptions there is a small narrow r wave (less than 0.04 seconds) in V1 to V3 which is not usually seen in anteroseptal infarction. There is also notching of the QRS best seen in the anterolateral leads, and the T wave goes in the opposite direction to the QRS in all the precordial leads. This combination of features is diagnostic. In the rare cases where there may be doubt assume the correct interpretation is LBBB. This will make up no difference to the administration of a thrombolytic on medical direction but for the present will be accepted as a contraindication for paramedics acting autonomously (see later slide). Right bundle branch block is characterised by QRS of 0.12 seconds or wider, an s wave in lead I, and a secondary R wave (R’) in V1. As abnormal Q waves do not occur with right bundle branch block, this remains a useful sign of infarction.

Sequence of changes in evolving AMI The ECG changes that occur due to myocardial infarction do not all occur at the same time. There is a progression of changes correlating to the progression of infarction. Within minutes of the clinical onset of infarction, there are no changes in the QRS complexes and therefore no definitive evidence of infarction. However, there is ST elevation providing evidence of myocardial damage. The next stage is the development of a new pathological Q wave and loss of the r wave. These changes occur at variable times and so can occur within minutes or can be delayed. Development of a pathological Q wave is the only proof of infarction. As the Q wave forms the ST elevation is reduced and after 1 week the ST changes tend to revert to normal, but the reduction in R wave voltage and the abnormal Q waves usually persist. The late change is the inversion of the T wave and in a non-Q wave myocardial infarct, when there is no pathological Q wave, this T wave change may be the only sign of infarction. Months after an MI the T waves may gradually revert to normal, but the abnormal Q waves and reduced voltage R waves persist. In terms of diagnosing AMI in time to make thrombolysis a life-saving possibility, the main change to look for on the ECG is ST segment elevation.

Location of infarction and its relation to the ECG: anterior infarction As was discussed in the previous module, the different leads look at different aspects of the heart, and so infarctions can be located by noting the changes that occur in different leads. The precordial leads (V1–6) each lie over part of the ventricular myocardium and can therefore give detailed information about this local area. aVL, I, V5 and V6 all reflect the anterolateral part of the heart and will therefore often show similar appearances to each other. II, aVF and III record the inferior part of the heart, and so will also show similar appearances to each other. Using these we can define where the changes will be seen for infarctions in different locations. Anterior infarctions usually occur due to occlusion of the left anterior descending coronary artery resulting in infarction of the anterior wall of the left ventricle and the intraventricular septum. It may result in pump failure due to loss of myocardium, ventricular septal defect, aneurysm or rupture and arrhythmias. ST elevation in I, aVL, and V2–6, with ST depression in II, III and aVF are indicative of an anterior (front) infarction. Extensive anterior infarctions show changes in V1–6 , I, and aVL.

Location of infarction and its relation to the ECG: inferior infarction ST elevation in leads II, III and aVF, and often ST depression in I, aVL, and precordial leads are signs of an inferior (lower) infarction. Inferior infarctions may occur due to occlusion of the right circumflex coronary arteries resulting in infarction of the inferior surface of the left ventricle, although damage can be made to the right ventricle and interventricular septum. This type of infarction often results in bradycardia due to damage to the atrioventricular node.

Location of infarction and its relation to the ECG: lateral infarction Occlusion of the left circumflex artery may cause lateral infarctions. Lateral infarctions are diagnosed by ST elevation in leads I and aVL.

Location of infarction: combinations The previous slides discussed the changes that occur in typical anterior, inferior and lateral infarctions. However, the area infarcted is not always limited to these areas and infarctions can extend across two regions. For example, an anterior infarction which is also on the lateral side of the heart is known as an anterolateral infarction. ST segment elevation in leads I and aVL represent a lateral infarction Anteroseptal infarctions show ST segment elevation in leads V1 to V4. ST elevation in V4 to V6 is typical of an anterolateral infarction ST elevation in II, III and aVF is typical of inferior infarction.

Diagnostic criteria for AMI Myocardial infarction is the loss of viable, electrically active myocardium. Diagnosis can therefore be made from the ECG. However, only changes in QRS complexes can provide a definite diagnosis. Changes in each of the leads must be noted, along with symptoms, as both are important in making a diagnosis. Excluding leads aVR and III, Q wave duration of more than 0.04 seconds or depth of more than 25% of the ensuing r wave are proof of infarction. Other criteria are the development of QS waves and local area low voltage r waves. Although these are useful diagnostic features, there are additional features that are associated with myocardial infarction as have been described in the previous slides. These include ST elevation in the leads facing the infarct, ST depression (reciprocal) in the opposite leads to the infarct, deep T wave inversion overlying and adjacent to the infarct, abnormally tall T waves facing the infarct, and cardiac arrhythmias. These extra features may aid in the diagnosis of myocardial infarction from an ECG.

This study evaluated the lipid profile in young Indian patients with angiographically proven CHD. Total cholesterol was found to be elevated in 54% of patients. Interestingly an equal proportion of patients had elevated triglycerides, HDL was found to be low in 60% of patients, while Lp(a) levels were elevated in 61% of patients. Thus the atherogenic phenotype B which is believed to be characteristic of diabetic patients seems to be prevalent even among Indian patients with CHD.

Risk factors for future cardiovascular events: WHS How well does the CRP test compare with other novel and emerging risk factors for vascular disease? This issue was directly addressed in the Women&apos;s Health Study, in this direct comparison of ten putative risk factors for vascular disease. In each case, the point estimate is based on being in the top versus bottom quartile for that particular analyte, and the horizontal bars represent the 95% confidence intervals for that effect. Starting from the top, we see that lipoprotein(a) screening was not a statistically significant predictor of risk, and below that, homocysteine screening, while statistically significant, was only of modest predictive value. This plot also indicates that the predictive value for LDL cholesterol, while highly statistically significant, sits approximately midway in terms of our overall risk prediction models. Interestingly, plasma levels of soluble intercellular adhesion molecule 1 (ICAM-1), a molecular marker associated with the adhesion and transmigration of leukocytes across the endothelial wall, as well as serum amyloid A (SAA), a nonspecific marker of inflammation, were in fact better markers of risk than was the LDL cholesterol or the total cholesterol level. Also of note from a clinical perspective, the best lipid marker was the total cholesterol:HDL cholesterol ratio. This finding is highly consistent with many prior epidemiologic studies and in fact is why many preventive practices prefer to use the ratio rather than any single lipid marker. However, the critical observation in this study was that plasma levels of hs-CRP on their own were actually the single strongest predictor for future vascular events, and those data are shown in the second line from the bottom. On its own, hs-CRP screening was associated with a 4.4-fold increase in risk for future vascular events among these otherwise healthy, middle-aged women. But again, the important issue is to consider combining the inflammatory screening with the lipid screening, and that is shown in the bottom line of data on the slide, suggesting that the combination of CRP level with total cholesterol: HDL cholesterol ratio provides the best overall risk estimate. Reference: Ridker PM, Hennekens CH, Buring JE, Rifai N. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med 2000;342:836-843.

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Our current understanding of the unstable coronary syndromes is that they fall on a spectrum of disease and begin with a coronary plaque rupture. The degree of thrombus determines the severity of the clinical syndrome, with total occlusion in ST elevation myocardial infarction (MI) or severe (90%) stenosis in patients with non-ST elevation MI or unstable angina. In addition, it is worthwhile to note that 99% of all plaque ruptures are clinically silent. A small degree of rupture leads to a small thrombus, which heals over, but leads to progression of the plaque—like rings on a tree. This is the understanding of how atherosclerosis progresses. This emphasizes the key role that antithrombotic therapy plays in all, patients with unstable coronary syndromes, both acutely and chronically.

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Antman and colleagues developed a simple risk scoring system to identify patients with various responses to treatments for unstable angina and non–ST-elevated myocardial infarction. It is characterized by its broad applicability and is easily calculated at patient presentation. The 7 Thrombolysis in Myocardial Infarction (TIMI) risk-score–predictor variables are aged &gt;65 years, unstable angina and &gt;3 risk factors for CAD, a prior stenosis of &gt;50%, aspirin in the past 7 days, &gt;2 anginal events in the prior 24 hours, ST-segment deviation on ECG at presentation, and elevated troponin. Event rates increased significantly as the TIMI risk score increased in a test cohort for TIMI IIB. The adverse event rates are significantly increased with a TIMI risk score of 4. Based on a TIMI risk score of 6, this combination of features indicates a high-risk patient.

Atherosclerotic disease is a progressive disease as shown in this slide. Many therapeutic interventions are aimed at specific cardiovascular conditions. These interventions may be directed at alleviating symptoms or preventing progression to more serious stages or both. Angiotensin-converting enzyme (ACE) inhibitors have been studied, for example, in patients with hypertension, who are at the top of this progression pathway. These studies looked only at the effects on blood pressure, however, and did not address the long-term question of risk reduction. Other clinical trials with ACE inhibitors have been designed to investigate the effects of these agents on the morbidity and mortality following an acute myocardial infarction.

Transcript of "Acute coronary syndromes in Indian context"

1.
ACS – INITIAL
DIAGNOSIS &
MANAGEMENT
Dr Uday Prashant M.D D.M

2.
Very Alarming Scene
• India is the Diabetic capital of the
world:- Highest no of diabetics in
world at present
• Indians have one of highest rates of
CAD
• Obesity in India is in rapid rise

3.
Coronary Artery Disease in
Indians = CADI
• How is it different from western world
• CADI strikes early !
• CADI strikes almost any one !!!
• CADI strikes unexpectedly !!!!
• Conventional RF can’t explain it away
• CADI is malignant in its onslaught.

4.
The CADI Volcano
• We are in the middle of the wave of CAD
epidemic
• This CADI epidemic will peak by 2015
• 50% deaths in India are CVD deaths.
• CADI will overtake Infectious diseases in
morbidity too
• By 2015 CADI will be six times more than the
West
• CADI will be 20 times more than the Chinese,

13.
Chest pain with ACS
• 15 -25 % of chest pain cases in ED
have ACS
• 2 % of ACS are missed
• These are current US data
• In India the percentages are far
higher
• For Pt mortality / for us medicolegal
implications

15.
Typical Angna
• Cardiac symptoms: Presence of acute chest,
epigastric, neck, jaw, or arm pain or
discomfort or pressure without apparent
noncardiac source.
• Levine`s sign may be +ve.
• More general, atypical symptoms, such as
fatigue, nausea, vomiting, diaphoresis,
faintness, and back pain, should not be used
as a diagnosis of Angina

17.
Epidemiological definition of MI
• Typical chest pain lasting for > 30
min not relieved by nitrates
• ECG showing characteristic changes
of MI
• Positive cardiac biomarkers of injury
WHO states any of two from above
three should be present.

37.
Homocysti(e)ne
• Normal value is up to 10 μ mols/L
• Excess of homocystine generates oxidative
stress on the cell membranes.
• Folic acid 5 mg/ day + Vit. B6 and B12 are
to be given on regular basis

45.
Management of MI
• All management strategies focus on
faster reperfusion of culprit artery.
• Spontaneous recanalization rates
after MI is
40 %
• But it is after 12 – 24 hrs
• Permanent damage has already set
in

46.
Management of MI
• Within 30 minutes if reperfused no
damage to myocardium.
• Within 2- 4 hrs of reperfusion the
damages are minimal.
• After 6 hrs what we save is much
less than what myocardium we loose

47.
Management of MI
• After 12 hrs no use of repurfusion
• permanent damage sets in though
surrounding hibernating myocardium can
be saved.
• To assess for hibernating myocardium we
have
Presence of chest pain
TMT
Nuclear Scans
Dobutamine Stress Echo
MRI etc

48.
• ITS NOT GIVING RIGHT TREATMENT
THAT IS IMPORTANT IN MI
MANAGEMENT BUT HOW FAST WE
ADMINISTER THAT IS IMPORTANT
• For every 30 min delay in reperfusion
the one year risk of relative mortality
increases by 8%

52.
Reperfusion Options for STEMI Patients
Step 2: Select Reperfusion Treatment.
If presentation is < 3 hours and there is no delay to an invasive strategy,
there is no preference for either strategy.
Invasive strategy generally preferred
 Skilled PCI lab available with surgical backup
 Door-to-balloon < 90 minutes
• High Risk from STEMI
 Cardiogenic shock, Killip class ≥ 3
 Contraindications to fibrinolysis, including
increased risk of bleeding and ICH
 Late presentation
 > 3 hours from symptom onset
 Diagnosis of STEMI is in doubt

53.
Fibrinolysis
I IIa IIb III
Fibrinolytic therapy should not be administered to
asymptomatic patients whose initial symptoms of
STEMI began more than 24 hours earlier.
I IIa IIb III
Fibrinolytic therapy should not be administered to
patients whose 12-lead ECG shows only STsegment depression, except if a true posterior MI
is suspected.

82.
Case of USA
•
•
•
•
Mr Sheik Ahhmed 45 yrs male
Chronic smoker
Labourer
For past 2 months not able to work due to
chest pain
• Somebody has to hit him in back for relief
of pain
• Increasing frequency & duration of pain

87.
Public Awareness
A survey of people with Diabetes
• Findings
– 68% do not consider cardiovascular
disease to be complication of diabetes
– 50%+ don’t feel risk for heart condition
or stroke
– 60% don’t feel at risk for high blood
pressure or cholesterol
– Awareness lowest among elderly,
minorities
2

88.
Why is CAD becoming so rampant
• Is it people are living longer?
• Is it increasing habits like smoking
cocaine?
• Is it raise in Diabetes?
• Is it food we eat?
• Or is it all in the genes?